Effect of acute hypoxia on vasopressin release and intravascular fluid during dynamic exercise in humans

Abstract

To test the hypothesis that acute hypoxia does not modify the relationship between plasma vasopressin concentration ([AVP]p) and plasma osmolality (Posmol) during exercise and that the increase in [AVP]p during exercise is due mainly to the exercise intensity-dependent increase in Posmol, we examined [AVP]p during a graded exercise in a hypoxic condition (13% O2, N2 balance) in seven healthy male subjects. A graded exercise in a normoxic condition on a separate day served as the control. Hypoxia reduced peak aerobic power (V˙o 2 peak) by 32.4 ± 2.7%. Blood samples obtained during rest and at around 25, 45, 65, 80, and 100% ofV˙o 2 peak of each of the respective conditions were used for analyses of intravascular water and electrolyte balance. The pattern of the changes in fluid and electrolyte balance in response to percentV˙o 2 peak was similar between the two conditions. Plasma volume decreased linearly as percentV˙o 2 peak increased while Posmol increased in a curvilinear fashion with a steep increase occurring at above ∼66%V˙o 2 peak. Above this relative exercise intensity, plasma sodium, potassium, and lactate concentrations also increased, whereas plasma bicarbonate concentration decreased. Thus transvascular fluid movement at above ∼66%V˙o 2 peak was due to the net efflux of hypotonic fluid out of the vascular space in both conditions. The relationship between [AVP]p and Posmol during exercise in response to relative exercise intensity was similar between the two conditions. The results indicate that acute mild hypoxia itself has no direct effect on vasopressin release, and it does not modify the relationship between [AVP]p and Posmol during exercise. The results also support the hypothesis that exercise-induced vasopressin release is primarily stimulated by increased Posmol produced by hypotonic fluid movement out of the vascular space in a relative exercise intensity-dependent manner.